Department of Physiology, Southern Illinois University, Carbondale, IL 62901, USA.
Endocrinology. 2022 Feb 1;163(2). doi: 10.1210/endocr/bqab263.
Understanding the molecular mechanisms underlying pituitary organogenesis and function is essential for improving therapeutics and molecular diagnoses for hypopituitarism. We previously found that deletion of the forkhead factor, Foxo1, in the pituitary gland early in development delays somatotrope differentiation. While these mice grow normally, they have reduced growth hormone expression and free serum insulin-like growth factor-1 (IGF1) levels, suggesting a defect in somatotrope function. FOXO factors show functional redundancy in other tissues, so we deleted both Foxo1 and its closely related family member, Foxo3, from the primordial pituitary. We find that this results in a significant reduction in growth. Consistent with this, male and female mice in which both genes have been deleted in the pituitary gland (dKO) exhibit reduced pituitary growth hormone expression and serum IGF1 levels. Expression of the somatotrope differentiation factor, Neurod4, is reduced in these mice. This suggests a mechanism underlying proper somatotrope function is the regulation of Neurod4 expression by FOXO factors. Additionally, dKO mice have reduced Lhb expression and females also have reduced Fshb and Prl expression. These studies reveal FOXO transcription factors as important regulators of pituitary gland function.
了解垂体器官发生和功能的分子机制对于改善垂体功能减退症的治疗和分子诊断至关重要。我们之前发现,在发育早期敲除垂体中的叉头框因子 Foxo1 会延迟生长激素细胞的分化。虽然这些小鼠正常生长,但它们的生长激素表达和游离血清胰岛素样生长因子 1(IGF1)水平降低,表明生长激素细胞功能缺陷。FOXO 因子在其他组织中表现出功能冗余,因此我们从原始垂体中敲除了 Foxo1 和其密切相关的家族成员 Foxo3。我们发现这会导致生长显著减少。与这一结果一致的是,在垂体中同时敲除这两个基因的雄性和雌性小鼠(dKO)表现出生长激素表达和血清 IGF1 水平降低。这些小鼠中的生长激素细胞分化因子 Neurod4 的表达减少。这表明,适当的生长激素细胞功能的机制是 FOXO 因子对 Neurod4 表达的调节。此外,dKO 小鼠的 Lhb 表达减少,雌性小鼠的 Fshb 和 Prl 表达也减少。这些研究揭示了 FOXO 转录因子是垂体功能的重要调节因子。